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FOODBORNE ILLNESS-TOXOPLASMA GONDII

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Toxoplasma gondii is a protozoan parasite, and is a common cause of human infection worldwide. Immunocompetent patients have mild, if any symptoms. Infection in utero or in an immunocompromised patient can cause severe effects.

Specific Substances

    1) Toxoplasmosis (synonym)
    2) Toxoplasma gondii (synonym)
    3) T. gondii (synonym)
    4) Food poisoning toxoplasma gondii (synonym)
    5) Toxoplasma gondii food poisoning (synonym)

Available Forms Sources

    A) FORMS
    1) Toxoplasma gondii is a protozoan parasite. It can infect most species of warm blooded animals, including humans, and can cause the disease toxoplasmosis. Immunocompetent patients are generally asymptomatic, although 10% to 20% may develop cervical lymphadenopathy or a flu-like illness that generally resolves within weeks to months. Immunocompromised patients (eg, AIDS, organ transplant) may develop retinochoroiditis, pneumonitis, or encephalitis (Centers for Disease Control and Prevention, 2009; McAuley, 2008). Toxoplasma gondii is the most significant of protozoan foodborne agents and it causes the greatest amount of parasitic infections. Although it has a low incidence, the disease burden of 620 disability-adjusted life-years per year is comparable to Salmonella species (670 disability-adjusted life-years per year) (Djurkovic-Djakovic et al, 2013).
    2) Acute infection in a pregnant woman can cause congenital toxoplasmosis in the fetus. Infection in the first trimester leads to congenital toxoplasmosis in 10% to 20% of cases, but manifestations can be severe including microcephaly, severe chorioretinitis, hearing loss and mental retardation (McAuley, 2008). Infection in the third trimester causes congenital infection in 80% to 90% of infants, but most are asymptomatic at birth though they may go on to develop ocular disease and may have subtle neurologic deficits (McAuley, 2008). Congenital T gondii infection can occur in approximately 5000 of 4.2 million babies born in the US (Djurkovic-Djakovic et al, 2013).
    B) SOURCES
    1) Domestic cats and their relatives are the only definitive hosts for Toxoplasma gondii. In the cat intestine, T. gondii undergoes sexual reproduction, resulting in the production of millions of oocysts that are relatively impervious to environmental degradation (Dabritz & Conrad, 2010). Unsporulated oocysts are shed in the cat's feces for approximately 1 to 2 weeks after infection. The oocysts may persist in the environment for months, once the oocysts sporulate they become infective. Animals that can serve as intermediate hosts (birds, rodents) may become infected after ingesting contaminated soil, or oocysts can contaminate water or plant material. Once ingested, oocysts transform into tachyzoites, which localize in neural or muscle tissue and develop into cyst bradyzoites. Cats that eat animals with tissue cysts then become acutely infected, or they may become infected by ingesting sporulated oocysts (eg, from contaminated water or plants). Wild game and animals bred for human consumption may also become infected and develop tissue cysts by ingesting sporulated oocysts (Centers for Disease Control and Prevention, 2009).
    2) Human infection can result from (Djurkovic-Djakovic et al, 2013; Dubey & Jones, 2008; Kijlstra & Jongert, 2008; Jones & Dubey, 2010; Petersen et al, 2010; Pereira et al, 2010; McAuley, 2008):
    1) Eating undercooked meat from animals with tissue cysts (ie, the meat from sheep, pigs, cows, chickens, goats, horses and wild game have been implicated)
    2) Ingesting food (ie, raw and unwashed fruits and vegetables) or water that is contaminated with cat feces
    3) Working in a contaminated environment (eg, cleaning a litter box, gardening in soil contaminated with cat feces)
    4) Ingesting unpasteurized milk and dairy products (eg, cow and goat milk have been implicated)
    5) Blood transfusion
    6) Organ transplant
    7) Transplacental (mother to fetus)
    3) Toxoplasmosis is a common infection worldwide. It is more prevalent in cultures that consume raw meat, and areas of the world where stray cats are common or the climate allows for the survival of oocysts and greater exposure to soil. In the US, serologic data suggests that about 22.5% of adolescents and adults have been infected (McAuley, 2008). It is usually a mild and self-limiting infection in immunocompetent individuals; however, newborns and immunocompetent individuals may develop more severe infection (Djurkovic-Djakovic et al, 2013).
    4) Toxoplasma gondii cysts in meat can be inactivated by freezing, heating, irradiation, and exposure to high pressure or acidity (Kijlstra & Jongert, 2008).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) CAUSATIVE ORGANISM
    1) Protozoan parasite: Toxoplasma gondii.
    B) EPIDEMIOLOGY
    1) One of the most common human infections throughout the world. About 22.5% of adolescents and adults in the US have serologic evidence of past infection. Incidence is higher in cultures that consume raw meat or climates that favor the survival of oocysts and exposure to contaminated soil.
    C) TARGET POPULATION
    1) All people are at risk of infection, but manifestations in an immunocompetent host are mild. Severe infections can occur in immunocompromised patients (eg, AIDS, organ transplant recipients, patients on high dose immunosuppression for connective tissue disorders). Congenital infection can cause severe, permanent sequelae in the infant.
    D) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) IMMUNOCOMPETENT PATIENTS: May be asymptomatic, or have mild manifestations such as headache, fever, malaise, myalgia, lymphadenitis, anorexia, arthralgias, vomiting, or rash. A minority may develop ocular infection. IMMUNOCOMPROMISED PATIENTS: May develop encephalitis (altered mental status, weakness, seizures, sensory abnormalities, cerebellar signs, meningitis, brain abscess, or diffuse brain lesions), and pneumonitis (cough, dyspnea, acute lung injury, respiratory failure), or disseminated toxoplasmosis with multi-organ involvement). CONGENITAL: Caused by acute maternal infection during pregnancy. Infection in the first trimester carries a lower risk of fetal transmission, but more severe effects such as intrauterine demise, microcephaly, mental retardation, seizures, blindness, hydrocephalus, intracranial calcifications, ascites, and hepatosplenomegaly. Maternal infection during the third trimester more often causes infection in the infant, but the manifestations are less severe (rash, lymphadenopathy, learning and visual deficits that may not be apparent until later in life). Patients with congenital toxoplasmosis may develop chorioretinitis decades after birth. OCULAR INVOLVEMENT: May develop in immunocompromised patients, in patients with congenital toxoplasmosis (but will usually not manifest until a decade or more after birth), and less often in immunocompetent adults either with reactivation of latent infection or during the acute infection. Manifestations my include varying degrees of visual loss, and anterior uveitis, vitreitis, cataracts, necrotizing retinitis, or retinal scars.
    2) ROUTE OF EXPOSURE
    a) Cats are the only definitive hosts for T. gondii. Food animals can become infected after exposure to plants, soil or water contaminated with cat feces. Humans can become infected from eating raw or undercooked meat, raw unwashed fruits and vegetables, unpasteurized milk or dairy products, drinking contaminated water, or by environmental contamination (cleaning a litter box, working with contaminated soil). Maternal to fetal transmission of acute infection occurs. Rarely, infection is transmitted by a blood transfusion or organ transplant.
    3) TIME TO ONSET
    a) The time to onset for acute infection is not known. Immunocompromised patients may develop reactivation of latent infection years after the initial illness. In transplant patients, the time from transplant to reactivation of latent toxoplasmosis is generally in the range of 2 to 4 months, although cases have been reported within 30 days and more than 6 months after transplant.
    0.2.20) REPRODUCTIVE
    A) Women who are infected prior to pregnancy generally do not pass the infection to their infants. Women who become infected while pregnant may pass the infection to the fetus. Maternal infections that occur during the first trimester have a lower risk of fetal transmission, but the effects on the fetus are more severe. Infections that occur during the third trimester are likely to be transmitted to the fetus, but the clinical events are less severe.

Laboratory Monitoring

    A) Diagnosis is usually made by detection of toxoplasma-specific IgG, IgM or IgA antibodies. If acute infection is suspected, test serum for IgG and IgM antibodies.
    B) Obtain a chest radiograph in patients with suspected pneumonitis.
    C) A brain CT should be performed on any patient with suspected CNS toxoplasmosis, but a normal CT does not exclude cerebral toxoplasma infection.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) IMMUNOCOMPETENT PATIENTS
    1) Most immunocompetent patients have self-limited lymphadenopathic toxoplasmosis, and treatment is NOT indicated. In rare cases, an immunocompetent patient with clinical evidence of visceral disease or symptoms that are severe or prolonged, a 2 to 4 week course of treatment is indicated. ADULT: PYRIMETHAMINE: Loading dose: 200 mg followed by 50 to 75 mg/day; PLUS SULFADIAZINE: 1 to 1.5 g 4 times daily; PLUS FOLINIC ACID (leucovorin): 10 to 25 mg with each dose of pyrimethamine. In patients with sulfa allergy, pyrimethamine plus clindamycin can be used. Fixed dose trimethoprim/sulfamethoxazole may be used when pyrimethamine is unavailable.
    B) CONGENITAL TOXOPLASMOSIS
    1) SUMMARY: Treatment of congenital toxoplasmosis requires 12 months of therapy. PYRIMETHAMINE: Loading dose: 2 mg/kg for 2 days, then 1 mg/kg daily for 6 months, then 1 mg/kg every Monday, Wednesday and Friday for 6 months; PLUS SULFADIAZINE: 100 mg/kg daily divided in 2 doses for 12 months; PLUS LEUCOVORIN: 10 mg 3 times a week for 12 months.
    C) PREGNANT PATIENT
    1) For pregnant women suspected of having acquired the infection at less than 18 weeks gestation: SPIRAMYCIN: 1 g (3 million units) every 8 hours until delivery (not commercially available in US, obtain from the National Collaborative Treatment Trial Study (773-834-4152)). For pregnant women suspected of having acquired the infection at or beyond 18 weeks of gestation, or with confirmed fetal infection (positive amniotic fluid polymerase chain reaction) or highly suspected (abnormalities on ultrasound consistent with fetal toxoplasmosis): PYRIMETHAMINE: 50 mg every 12 hours for 2 days followed by 50 mg daily; PLUS SULFADIAZINE: Initial dose: 75 mg/kg, followed by 50 mg/kg every 12 hours (maximum 4 g/day); PLUS FOLINIC ACID (leucovorin): 10 to 20 mg daily (during and 1 week after completion of pyrimethamine therapy).
    D) OCULAR TOXOPLASMOSIS
    1) ADULT: PYRIMETHAMINE: 200 mg loading dose on the first day followed by 75 mg/day; PLUS SULFADIAZINE: 1 g 4 times daily; PLUS FOLINIC ACID (leucovorin): 15 mg/day with each dose of pyrimethamine.
    2) PEDIATRIC: PYRIMETHAMINE: Loading dose: 2 mg/kg (max 200 mg) followed by 1 mg/kg daily (max 75 mg); PLUS SULFADIAZINE: 100 mg/kg daily (max 1500 mg); PLUS LEUCOVORIN: 10 to 20 mg 3 times a week. PREDNISONE: 1 mg/kg daily is also given, if lesions threaten vision. Treatment is continued until 1 to 2 weeks after symptoms resolve.
    E) IMMUNOCOMPROMISED PATIENTS
    1) SUMMARY: Several regimens are available. Treatment is continued for 4 to 6 weeks after signs and symptoms resolve.
    2) ADULT: PYRIMETHAMINE (Standard regimen): Loading dose: 200 mg followed by 50 to 75 mg/day; PLUS SULFADIAZINE: 1 to 1.5 g orally 4 times daily; PLUS FOLINIC ACID (leucovorin): 10 to 25 mg orally with each dose of pyrimethamine.
    3) CLINDAMYCIN (Alternative standard regimen): 600 mg orally or IV every 6 hours.
    4) TRIMETHOPRIM-SULFAMETHOXAZOLE (possible alternative regimen): 5 mg/kg of the trimethoprim component orally or IV every 12 hours (doses up to 15 to 20 mg/kg/day of the trimethoprim component have been used).
    5) OTHER: Pyrimethamine plus folinic acid (as a standard regimen) has also been used in combination with ONE of the following: ATOVAQUONE: 1500 mg orally every 12 hours (or 750 mg every 6 hours); OR CLARITHROMYCIN: 500 mg orally every 12 hours; OR AZITHROMYCIN: 900 to 1200 mg orally daily; OR CLINDAMYCIN: 600 mg IV every 6 hours (or 450 mg orally 4 times daily); OR DAPSONE: 100 mg orally daily.
    F) DIFFERENTIAL DIAGNOSIS
    1) Mononucleosis, cytomegalovirus infection, lymphoma, tuberculosis, tularemia.
    G) PITFALLS
    1) Primary pitfall is attributing signs and symptoms to another cause. Disseminated disease in immunocompromised patients is often fatal, if not treated early.

Range Of Toxicity

    A) The infectious dose is not known.

Clinical Effects

Summary Of Exposure

    A) CAUSATIVE ORGANISM
    1) Protozoan parasite: Toxoplasma gondii.
    B) EPIDEMIOLOGY
    1) One of the most common human infections throughout the world. About 22.5% of adolescents and adults in the US have serologic evidence of past infection. Incidence is higher in cultures that consume raw meat or climates that favor the survival of oocysts and exposure to contaminated soil.
    C) TARGET POPULATION
    1) All people are at risk of infection, but manifestations in an immunocompetent host are mild. Severe infections can occur in immunocompromised patients (eg, AIDS, organ transplant recipients, patients on high dose immunosuppression for connective tissue disorders). Congenital infection can cause severe, permanent sequelae in the infant.
    D) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) IMMUNOCOMPETENT PATIENTS: May be asymptomatic, or have mild manifestations such as headache, fever, malaise, myalgia, lymphadenitis, anorexia, arthralgias, vomiting, or rash. A minority may develop ocular infection. IMMUNOCOMPROMISED PATIENTS: May develop encephalitis (altered mental status, weakness, seizures, sensory abnormalities, cerebellar signs, meningitis, brain abscess, or diffuse brain lesions), and pneumonitis (cough, dyspnea, acute lung injury, respiratory failure), or disseminated toxoplasmosis with multi-organ involvement). CONGENITAL: Caused by acute maternal infection during pregnancy. Infection in the first trimester carries a lower risk of fetal transmission, but more severe effects such as intrauterine demise, microcephaly, mental retardation, seizures, blindness, hydrocephalus, intracranial calcifications, ascites, and hepatosplenomegaly. Maternal infection during the third trimester more often causes infection in the infant, but the manifestations are less severe (rash, lymphadenopathy, learning and visual deficits that may not be apparent until later in life). Patients with congenital toxoplasmosis may develop chorioretinitis decades after birth. OCULAR INVOLVEMENT: May develop in immunocompromised patients, in patients with congenital toxoplasmosis (but will usually not manifest until a decade or more after birth), and less often in immunocompetent adults either with reactivation of latent infection or during the acute infection. Manifestations my include varying degrees of visual loss, and anterior uveitis, vitreitis, cataracts, necrotizing retinitis, or retinal scars.
    2) ROUTE OF EXPOSURE
    a) Cats are the only definitive hosts for T. gondii. Food animals can become infected after exposure to plants, soil or water contaminated with cat feces. Humans can become infected from eating raw or undercooked meat, raw unwashed fruits and vegetables, unpasteurized milk or dairy products, drinking contaminated water, or by environmental contamination (cleaning a litter box, working with contaminated soil). Maternal to fetal transmission of acute infection occurs. Rarely, infection is transmitted by a blood transfusion or organ transplant.
    3) TIME TO ONSET
    a) The time to onset for acute infection is not known. Immunocompromised patients may develop reactivation of latent infection years after the initial illness. In transplant patients, the time from transplant to reactivation of latent toxoplasmosis is generally in the range of 2 to 4 months, although cases have been reported within 30 days and more than 6 months after transplant.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) In a series of 426 patients with serologic evidence of recent Toxoplasma gondii infection from a municipal water supply, 155 (36%) had symptoms; 128 patients (30%) reported fever (Dodds, 2006).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) OCULAR TOXOPLASMOSIS
    a) Ocular toxoplasmosis can develop in patients with congenital toxoplasmosis, although clinical manifestations may be delayed until adolescence or young adulthood. It develops with reactivation of latent infection or acute infection in immunocompromised patients. It may also develop in a minority of immunocompetent patients with acute infection (Pereira et al, 2010).
    b) Clinical manifestations include photophobia, floaters, and varying severity of visual loss. It is the most common infectious cause of visual impairment or blindness in the developed world (Pereira et al, 2010).
    c) On physical exam, anterior uveitis, vitreitis, cataracts, and elevated intraocular pressure may be noted (Dodds, 2006; Delair et al, 2011).
    d) Findings on fundoscopic exam can include: swelling of the optic disc, white areas of retinochoroiditis, necrotizing retinitis, atrophic retinochoroidal scars, macular detachment and macular exudates (Garza-Leon et al, 2008; Dodds, 2006; Delair et al, 2011).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) PNEUMONITIS
    1) WITH POISONING/EXPOSURE
    a) Pneumonitis can develop in immunocompromised patients. Manifestations include fever, cough, dyspnea, and respiratory failure. Many of these patients will also have disseminated toxoplasma infection of other organs (Derouin & Pelloux, 2008).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) ENCEPHALITIS
    1) WITH POISONING/EXPOSURE
    a) Encephalitis is the most common presentation of Toxoplasma infection in patients with HIV/AIDS. Clinical manifestations are myriad and can include: headaches, fever, altered mental status, confusion, focal neurologic findings such as weakness or sensory changes, seizures, cerebellar dysfunction, and neuropsychiatric changes (Lee et al, 2009; Weenink et al, 2009; Montoya et al, 2010).
    b) Cerebrospinal fluid analysis may be normal, or may show elevated protein and mononuclear pleocytosis, usually with lymphocyte predominance. Hypoglycorrhachia is uncommon (Montoya et al, 2010).
    c) Brain CT or MRI may show single or multiple lesions that are isodense or hypodense, with some mass effects, and contrast enhancement in a ring-like or nodular pattern (Montoya et al, 2010).
    d) Encephalitis is the most common presentation of toxoplasmosis in transplant recipients. It usually represents reactivation of latent infection, and is most common in patients who have received allogenic hematologous stem cell transplantation. Most cases develop within 2 to 3 months post transplant, but has been reported within the first month and more than 6 months after transplant (Derouin & Pelloux, 2008)
    B) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) In a series of 426 patients with serologic evidence of recent Toxoplasma gondii infection from a municipal water supply, 155 (36%) had symptoms; 135 patients (32%) reported headache (Dodds, 2006).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) In a series of 426 patients with serologic evidence of recent Toxoplasma gondii infection from a municipal water supply, 155 (36%) had symptoms; 60 (14%) patients reported vomiting and 107 (25%) reported anorexia (Dodds, 2006).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) HEPATOSPLENOMEGALY
    1) WITH POISONING/EXPOSURE
    a) Hepatosplenomegaly and jaundice may be manifestations of congenital toxoplasmosis (Tamma, 2007).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) WITH POISONING/EXPOSURE
    a) Maculopapular rash can be a manifestation of congenital toxoplasmosis, or acute infection, but it is not common (Tamma, 2007).
    b) In a series of 426 patients with serologic evidence of recent Toxoplasma gondii infection from a municipal water supply, 155 (36%) had symptoms; 11 patients (2.6%) had a rash (Dodds, 2006).
    B) NIGHT SWEATS
    1) WITH POISONING/EXPOSURE
    a) In a series of 426 patients with serologic evidence of recent Toxoplasma gondii infection from a municipal water supply, 155 (36%) had symptoms; 83 patients (19%) reported night sweats (Dodds, 2006).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) In a series of 426 patients with serologic evidence of recent Toxoplasma gondii infection from a municipal water supply, 155 (36%) had symptoms; 124 patients (29%) complained of myalgia and 95 (22%) reported arthralgia (Dodds, 2006).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) LYMPHADENITIS
    1) WITH POISONING/EXPOSURE
    a) Lymphadenitis may be a manifestation of acute or congenital toxoplasmosis (Tamma, 2007).
    b) In a series of 426 patients with serologic evidence of recent Toxoplasma gondii infection from a municipal water supply, 155 (36%) had symptoms; 117 patients (27%) had lymphadenitis (Dodds, 2006).

Reproductive

    3.20.1) SUMMARY
    A) Women who are infected prior to pregnancy generally do not pass the infection to their infants. Women who become infected while pregnant may pass the infection to the fetus. Maternal infections that occur during the first trimester have a lower risk of fetal transmission, but the effects on the fetus are more severe. Infections that occur during the third trimester are likely to be transmitted to the fetus, but the clinical events are less severe.
    3.20.2) TERATOGENICITY
    A) FIRST TRIMESTER INFECTION
    1) Maternal infection in the first trimester leads to congenital toxoplasmosis in approximately 10% to 20% of cases, however, the manifestations are severe including microcephaly, severe chorioretinitis, hearing loss and mental retardation (McAuley, 2008).
    B) SECOND TRIMESTER INFECTION
    1) Maternal infection in the second trimester leads to congenital toxoplasmosis in about 40% of infants, with about 25% manifesting clinical symptoms (Montoya & Remington, 2008).
    C) THIRD TRIMESTER INFECTION
    1) Infection in the third trimester causes congenital infection in 80% to 90% of infants, but most are asymptomatic at birth though they may go on to develop ocular disease and may have subtle neurologic defects (McAuley, 2008).
    D) ONSET OF SYMPTOMS
    1) Most infants with congenital toxoplasmosis are asymptomatic at birth or during the neonatal period. They may develop evidence of chorioretinitis years or decades later, and may have subtle neurologic defects. A small minority of infants have symptoms at birth or in the immediate neonatal period, while others have symptoms within the first few weeks or months of life (Kaye, 2011).
    2) The classic triad of congenital toxoplasmosis is hydrocephalus, retinochoroiditis, and central nervous system calcifications, but it is only present in a minority of patients. Signs and symptoms include seizures, cranial nerve palsies, motor weakness, delays in growth or mental retardation, visual or hearing impairment, learning disabilities, lymphadenopathy, fever, organomegaly or rash, but the onset or signs and symptoms are often delayed beyond the neonatal period (Kaye, 2011).
    3.20.3) EFFECTS IN PREGNANCY
    A) IMMUNOCOMPROMISED MOTHERS
    1) Women who are infected prior to pregnancy generally do not pass the infection to their offspring. Women who are severely immunocompromised (ie, HIV/AIDS, high-dose immunosuppressive therapy for organ transplant, malignancy or connective tissue disorders) can have reactivation of latent infection while pregnant, and this can cause fetal toxoplasmosis (Montoya & Remington, 2008).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Toxoplasma gondii tachyzoites can be present in the colostrum and breast milk of nursing mothers with primary T. gondii infection, and ingestion of the milk can induce infection in the nursing infant (Pereira et al, 2010).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Diagnosis is usually made by detection of toxoplasma-specific IgG, IgM or IgA antibodies. If acute infection is suspected, test serum for IgG and IgM antibodies.
    B) Obtain a chest radiograph in patients with suspected pneumonitis.
    C) A brain CT should be performed on any patient with suspected CNS toxoplasmosis, but a normal CT does not exclude cerebral toxoplasma infection.
    4.1.2) SERUM/BLOOD
    A) Diagnosis is usually made by detection of toxoplasma-specific IgG, IgM or IgA antibodies. If acute infection is suspected, test serum for IgG and IgM antibodies. Several antibody tests can also be used within the first several weeks of infection: dye test, indirect fluorescent antibody test, and enzyme immunoassays (Centers for Disease Control and Prevention, 2010). IgG may be positive for decades, while IgM generally persists for 6 to 9 months and is a better marker of recent infection (Pereira et al, 2010).
    B) Serologic tests may be unreliable in immunocompromised patients. Polymerase chain reaction is often used in these patients, and is also used on amniotic fluid to evaluate for fetal infection (Centers for Disease Control and Prevention, 2010; Abdul-Ghani, 2011).
    C) Direct visualization of the parasite in stained tissue sections, cerebrospinal fluid (CSF) or biopsy specimens is occasionally performed. Rarely, toxoplasma gondii is isolated from the blood or CSF, but it is difficult and time consuming (Centers for Disease Control and Prevention, 2010). Toxoplasma gondii can be isolated from the placenta in about 95% of newborns with congenital toxoplasmosis, but it can also be isolated in noninfected infants (McAuley, 2008).
    D) In some areas of the world, pregnant women are screened for evidence of previous Toxoplasma gondii infection at the first prenatal visit. Patients with no evidence of previous infection are then tested monthly or every 3 months for evidence of seroconversion, which suggests acute infection. Women with positive initial serology may undergo further testing to evaluate for recent infection. If acute infection is diagnosed, the woman is treated and undergoes amniocentesis after 14 weeks gestation to evaluate for evidence of fetal infection (Khoshnood et al, 2007).
    4.1.4) OTHER
    A) OTHER
    1) Ocular toxoplasmosis can be difficult to diagnosis, as serologic tests may be negative. The diagnosis is largely based on clinical presentation. Analysis of the vitreous or aqueous humor for the presence of anti-Toxoplasma antibodies and T. gondii DNA by polymerase chain reaction is sometimes performed, if the diagnosis is unclear (Garweg et al, 2011).
    2) Toxoplasmosis in transplant patients usually results from reactivation of latent infection, and serologic tests are difficult to interpret. Diagnosis often depends on the identification of the parasite or its DNA in blood, bone marrow, cerebrospinal fluid, bronchoalveolar lavage fluid or biopsy specimens (Derouin & Pelloux, 2008).
    3) Lumbar puncture should be performed in any patient with suspected Toxoplasma encephalitis. CSF may be normal, but typically shows pleocytosis with lymphocytic predominance and elevated protein. In infants with congenital toxoplasmosis, the CSF protein may be markedly elevated (Montoya et al, 2010).

Radiographic Studies

    A) Obtain a chest radiograph in patients with suspected pneumonitis.
    B) A brain CT should be performed on any patient with suspected CNS toxoplasmosis, but a normal CT does not exclude cerebral toxoplasma infection (Weenink et al, 2009).
    1) Brain CT or MRI may show single or multiple lesions that are isodense or hypodense, with some mass effects, and contrast enhancement in a ring-like or nodular pattern (Montoya et al, 2010).
    C) Infants with congenital toxoplasmosis may have evidence of CNS calcification on cranial ultrasound (Montoya et al, 2010).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Diagnosis is usually made by detection of toxoplasma-specific IgG, IgM or IgA antibodies. If acute infection is suspected, test serum for IgG and IgM antibodies.
    B) Obtain a chest radiograph in patients with suspected pneumonitis.
    C) A brain CT should be performed on any patient with suspected CNS toxoplasmosis, but a normal CT does not exclude cerebral toxoplasma infection.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) GI decontamination is not indicated. Vomiting is likely to occur following an acute exposure.
    6.5.2) PREVENTION OF ABSORPTION
    A) GI decontamination is not indicated. Vomiting is likely to occur following an acute exposure.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Diagnosis is usually made by detection of toxoplasma-specific IgG, IgM or IgA antibodies. If acute infection is suspected, test serum for IgG and IgM antibodies.
    2) Obtain a chest radiograph in patients with suspected pneumonitis.
    3) A brain CT should be performed on any patient with suspected CNS toxoplasmosis, but a normal CT does not exclude cerebral toxoplasma infection.
    B) IMMUNOCOMPETENT
    1) Most immunocompetent patients have self-limited lymphadenopathic toxoplasmosis, and treatment is NOT indicated. In rare cases, immunocompetent patients with clinical evidence of visceral disease or symptoms that are severe or prolonged, a 2 to 4 week course of treatment is indicated (Centers for Disease Control and Prevention, 2010).
    a) ADULT: PYRIMETHAMINE: Loading dose: 200 mg, followed by 50 to 75 mg/day; PLUS SULFADIAZINE: 1 to 1.5 g 4 times daily; PLUS FOLINIC ACID (leucovorin): 10 to 25 mg with each dose of pyrimethamine. In patients with sulfa allergy, pyrimethamine plus clindamycin can be used. Fixed dose trimethoprim/sulfamethoxazole may be used when pyrimethamine is unavailable (Centers for Disease Control and Prevention, 2010).
    C) CONGENITAL TOXOPLASMOSIS
    1) Treatment of congenital toxoplasmosis requires 12 months of therapy. The following regimen has shown that children treated postnatally with this regimen have significantly better visual and neurodevelopmental outcomes than historical controls. Infants should be monitored for bone marrow toxicity (McAuley, 2008).
    a) PYRIMETHAMINE: LOADING DOSE: 2 mg/kg for 2 days, then 1 mg/kg daily for 6 months, then 1 mg/kg every Monday, Wednesday and Friday for 6 months; PLUS SULFADIAZINE: 100 mg/kg daily divided in 2 doses for 12 months; PLUS LEUCOVORIN: 10 mg 3 times a week for 12 months (McAuley, 2008).
    D) PATIENT CURRENTLY PREGNANT
    1) For pregnant women suspected of having acquired the infection at less than 18 weeks gestation: SPIRAMYCIN: 1 g (3 million units) every 8 hours until delivery (not commercially available in US, obtain from the National Collaborative Treatment Trial Study (773-834-4152)) (Montoya & Remington, 2008).
    2) For pregnant women suspected of having acquired the infection at or beyond 18 weeks of gestation, or with confirmed fetal infection (positive amniotic fluid polymerase chain reaction) or highly suspected (abnormalities on ultrasound consistent with fetal toxoplasmosis): PYRIMETHAMINE: 50 mg every 12 hours for 2 days followed by 50 mg daily; PLUS SULFADIAZINE: Initial dose: 75 mg/kg, followed by 50 mg/kg every 12 hours (maximum 4 g/day); PLUS FOLINIC ACID (leucovorin): 10 to 20 mg daily (during and 1 week after completion of pyrimethamine therapy) (Montoya & Remington, 2008).
    3) In a systematic review of cohort studies involving 1438 mothers identified with toxoplasmosis by prenatal screening, there was weak evidence that maternal treatment started within 3 weeks of seroconversion reduced mother-to-infant transmission of disease (adjusted odds ratio 0.48, 95% confidence interval 0.28 to 0.80, p=0.05). There was no evidence that maternal treatment reduced the risk of clinical manifestations in the child (Thiebaut et al, 2007).
    E) OCULAR TOXOPLASMOSIS
    1) ADULTS
    a) PYRIMETHAMINE: 200 mg loading dose on the first day followed by 75 mg/day, PLUS SULFADIAZINE 1 g 4 times daily; PLUS FOLINIC ACID (leucovorin) 15 mg/day with each dose of pyrimethamine (de-la-Torre et al, 2011).
    b) Alternative regimens include: TRIMETHOPRIM 160 mg and SULFAMETHOXAZOLE 800 mg every 12 hours for 6 weeks; OR AZITHROMYCIN 500 mg/day for 5 weeks; OR Intravitreal CLINDAMYCIN 1 mg injection and dexamethasone 400 mcg as a single dose (de-la-Torre et al, 2011).
    2) CHILDREN
    a) PYRIMETHAMINE: 2 mg/kg loading dose (maximum: 200 mg) followed by 1 mg/kg daily (maximum: 75 mg); PLUS SULFADIAZINE: 100 mg/kg daily (maximum: 1500 mg); PLUS LEUCOVORIN: 10 to 20 mg 3 times a week. PREDNISONE: 1 mg/kg daily is also given if lesions threaten vision. Treatment is continued until 1 to 2 weeks after symptoms resolve (McAuley, 2008).
    b) An alternative regimen includes azithromycin 10 mg/kg/day for 2 months (de-la-Torre et al, 2011).
    F) MULTISYSTEMIC DISSEMINATED TOXOPLASMOSIS
    1) TOXOPLASMOSIS IN THE IMMUNOCOMPROMISED PATIENT
    a) Several regimens are available. Treatment is continued for 4 to 6 weeks after signs and symptoms resolve.
    b) PYRIMETHAMINE (standard regimen): ADULT: 200 mg loading dose followed by 50 to 75 mg/day; PLUS SULFADIAZINE: 1 to 1.5 g orally 4 times daily; PLUS FOLINIC ACID (leucovorin): 10 to 25 mg orally once a day (Kappagoda et al, 2011; Montoya et al, 2010).
    c) CLINDAMYCIN (alternative standard regimen): 600 mg orally or IV (up to 1200 mg IV) every 6 hours (Montoya et al, 2010) .
    d) TRIMETHOPRIM-SULFAMETHOXAZOLE (possible alternative regimen): 5 mg/kg of the trimethoprim component orally or IV every 12 hours (doses up to 15 to 20 mg/kg/day of the trimethoprim component have been used) (Kappagoda et al, 2011; Montoya et al, 2010).
    e) OTHER: Pyrimethamine plus folinic acid (as a standard regimen) has also been used in combination with ONE of the following: ATOVAQUONE: 1500 mg orally every 12 hours (or 750 mg every 6 hours); OR CLARITHROMYCIN: 500 mg orally every 12 hours; OR AZITHROMYCIN: 900 to 1200 mg orally daily; OR CLINDAMYCIN: 600 mg IV every 6 hours (or 450 mg orally 4 times daily); OR DAPSONE: 100 mg orally daily (Kappagoda et al, 2011; Montoya et al, 2010).

Range Of Toxicity

Summary

    A) The infectious dose is not known.

References

General Bibliography

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